Study examines use of bitter substances to halt preterm labor

Ronghua ZhuGe and colleagues found that exposing bitter taste receptors in the uterus to bitter substances may stop contractions

UMass Medical School Communications

July 25, 2017
  Ronghua ZhuGe, PhD
 

Ronghua ZhuGe, PhD

New research by Ronghua ZhuGe, PhD, associate professor of microbiology & physiological systems, and colleagues offers insight into the mechanisms of uterine contractions during labor and may lead to new treatments to reduce instances of preterm birth, a leading cause of neonatal mortality and morbidity.

In a study published in The FASEB Journal, Dr. ZhuGe and colleagues found that exposing bitter taste receptors (TAS2Rs) in the uterus to certain substances may stop contractions that occur during premature labor. 

“The biological mechanism of labor initiation remains unknown, and a large percentage of preterm pregnancies do not respond well to current medications,” said ZhuGe, senior author on the study.

“The bitter taste receptors that we have found on uterine muscle could be one more piece of the puzzle to understand the onset of labor, both at term and preterm, and develop new therapeutics for preterm labor,” ZhuGe said.

ZhuGe and colleagues from UMass Medical School, University of Rhode Island, Wayne State University, and the College of Animal Science and Technology in China examined human and mouse uterine myometrium tissue (also known as smooth muscle). The researchers first exposed the tissue to native hormones such as oxytocin and chemical compounds to make it contract, mimicking normal or premature labor. They then exposed the tissue to bitter substances.

By activating the bitter taste receptors in the uterus, the bitter substances relaxed the contracted uterine muscle tissue more completely than the current drugs used to prevent preterm labor in humans. The researchers also found that giving mice bitter substances before they showed any premature contractions prevented them from having early deliveries, and this protection is largely lost in mice without a functioning TAS2R signaling pathway.

“Collectively, our results reveal that activation of the canonical TAS2R signaling system in myometrial cells produces profound relaxation of myomentrium precontracted by a broad spectrum of contractile agonists, and that targeting TAS2Rs is an attractive approach to developing effective tocolytics for preterm birth management,” ZhuGe said.

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